Cellular and molecular characterization of oxidative stress in olfactory epithelium of Harlequin mutant mouse

Vaishnav, Radhika A.; Getchell, Marilyn L.; Huang, Liping; Hersh, Matthew A.; Stromberg, Arnold J.; Getchell, Thomas V.

doi:10.1002/jnr.21464

Cited by 14 publications

(10 citation statements)

References 109 publications

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“…In mice, various spontaneous mutant strains similarly display progressive cerebellar and retinal degeneration, including nervous , harlequin , and Purkinje cell degeneration ( pcd ) Mullen et al (1976), LaVail et al (1993), Vaishnav et al (2008). For this reason, fundamental processes of neuron development and neuron survival are likely to be shared between the cerebellum and retina, providing an opportunity to delineate such pathways by comparative analysis of the molecular basis of cerebellar and retinal degeneration involving such mutations.…”

Section: Discussionmentioning

confidence: 99%

The zinc-binding domain of Nna1 is required to prevent retinal photoreceptor loss and cerebellar ataxia in Purkinje cell degeneration (pcd) mice

et al. 2008

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The Purkinje cell degeneration (pcd) mouse undergoes retinal photoreceptor degeneration and Purkinje cell loss. Nna1 is postulated to be the causal gene for pcd. We show that a BAC containing the Nna1 gene rescues retinal photoreceptor loss and Purkinje cell degeneration, confirming that Nna1 loss-of-function is responsible for these phenotypes. Mutation of the zinc-binding domain within the transgene destroyed its ability to rescue neuronal loss in pcd5J homozygous mice. In conclusion, Nna1 is required for survival of retinal photoreceptors and other neuron populations that degenerate in pcd mice. A functional zinc-binding domain is crucial for Nna1 to support neuron survival.

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Section: Discussionmentioning

confidence: 99%

The zinc-binding domain of Nna1 is required to prevent retinal photoreceptor loss and cerebellar ataxia in Purkinje cell degeneration (pcd) mice

et al. 2008

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“…This suggested the role of oxidative mechanisms influencing risk and progression of Alzheimer's disease [60,93].…”

Section: Alzheimer's and Parkinson's Diseasesmentioning

confidence: 96%

The Versatile Stress Protein Mortalin as a Chaperone Therapeutic Agent

Deocaris

Kaul²,

Wadhwa³

2009

PPL

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Age- and stress-induced modulations in chaperone systems result in "chaperono-deficiency" or "chaperon-opulence". Development of modulators, of chaperone function has therefore, become an emerging field in drug development and discovery. This mini-review summarizes (i) the events leading to identification of an Hsp70 family stress chaperone, mortalin, (ii) experimental evidence to its role in old age diseases and cancer, and (iii) proposes it as a chaperono-therapeutic agent. As post-translational modifications and expression changes in mortalin are being explored as a biomarker for cancer, cardiovascular diseases and neurodegeneration, we discuss here how the current tools used in studying mortalin (e.g. antibodies, peptides, ribozymes, antisense and siRNA, recombinant proteins and small molecules etc.) could be creatively applied in a clinical setting to manage stress and to treat various chaperone-based maladies or "chaperonopathies".

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“…In the OB, autofluorescent structures were observed in tissue from mice that received intranasal saline or MSC-EGFPs, and also from mice that did not receive any intranasal treatment, suggesting that physical stress caused by intranasal injections is not the cause of OB autoflourescence. Little is known about autofluorescence in the OB, but two reports describe naturally occurring lipofuscin in the OB and its relationship to oxidative enzymatic activity [38, 39]. …”

Section: Discussionmentioning

confidence: 99%

Detection of Intranasally Delivered Bone Marrow-Derived Mesenchymal Stromal Cells in the Lesioned Mouse Brain: A Cautionary Report

Chartoff

Damez-Werno²,

Sonntag³

et al. 2011

Stem Cells International

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Bone marrow-derived mesenchymal stromal cells (MSCs) hold promise for autologous treatment of neuropathologies. Intranasal delivery is relatively noninvasive and has recently been reported to result in transport of MSCs to the brain. However, the ability of MSCs to migrate from nasal passages to sites of neuropathology and ultimately survive has not been fully examined. In this paper, we harvested MSCs from transgenic mice expressing enhanced green fluorescent protein (cells hereafter referred to as MSC-EGFP) and delivered them intranasally to wild-type mice sustaining mechanical lesions in the striatum. Using fluorescent, colorimetric, and ultrastructural detection methods, GFP-expressing cells were undetectable in the brain from 3 hours to 2 months after MSC delivery. However, bright autofluorescence that strongly resembled emission from GFP was observed in the olfactory bulb and striatum of lesioned control and MSC-EGFP-treated mice. In a control experiment, we directly implanted MSC-EGFPs into the mouse striatum and detected robust GFP expression 1 and 7 days after implantation. These findings suggest that—under our conditions—intranasally delivered MSC-EGFPs do not survive or migrate in the brain. Furthermore, our observations highlight the necessity of including appropriate controls when working with GFP as a cellular marker.

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Cellular and molecular characterization of oxidative stress in olfactory epithelium of Harlequin mutant mouse

Cited by 14 publications

References 109 publications

The zinc-binding domain of Nna1 is required to prevent retinal photoreceptor loss and cerebellar ataxia in Purkinje cell degeneration (pcd) mice

The zinc-binding domain of Nna1 is required to prevent retinal photoreceptor loss and cerebellar ataxia in Purkinje cell degeneration (pcd) mice

The Versatile Stress Protein Mortalin as a Chaperone Therapeutic Agent

Detection of Intranasally Delivered Bone Marrow-Derived Mesenchymal Stromal Cells in the Lesioned Mouse Brain: A Cautionary Report

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